Abstract
Elevated plasma fibrinogen levels and tumor progression in patients with gastric cancer (GC) have been largely reported. However, distinct fibrinogen chains and domains have different effects on coagulation, inflammation, and angiogenesis. The aim of this study was to characterize fibrinogen β chain (FGB) in GC tissues. Retrospectively we analyzed the data of matched pairs of normal (N) and malignant tissues (T) of 28 consecutive patients with GC at diagnosis by combining one- and two-dimensional electrophoresis (1DE and 2DE) with immunoblotting and mass spectrometry together with two-dimensional difference in gel electrophoresis (2D-DIGE). 1DE showed bands of the intact FGB at 50 kDa and the cleaved forms containing the fragment D at ~37–40 kDa, which corresponded to 19 spots in 2DE. In particular, spot 402 at ~50 kDa and spots 526 and 548 at ~37 kDa were of interest by showing an increased expression in tumor tissues. A higher content of spot 402 was associated with stomach antrum, while spots 526 and 548 amounts correlated with corpus and high platelet count (>208 × 109/L). The quantification of FGB and cleaved products may help to further characterize the interconnections between GC and platelet/coagulation pathways.
Highlights
Gastric cancer (GC) is the fifth most common cancer and the third leading cause of cancer death in the world [1]
Proteomics provided consistent information in revealing proteome alterations associated with GC, dissected some of the mechanisms underlying gastric cancerogenesis, and enabled the identification of several diagnostic, prognostic, and predictive biomarkers [6,7,8,9]
The FGB forms we found may represent new candidate molecules for GC diagnosis, which could be further exploited in terms of possible interconnections between cancer and platelet/coagulation pathways
Summary
Gastric cancer (GC) is the fifth most common cancer and the third leading cause of cancer death in the world [1]. There is a great interest in deciphering the molecular pathways associated with its progression and prognosis. Environment and lifestyles are general risk factors for GC, but interaction of diet with multiple genetic and epigenetic alterations occur during GC development [2,3,4,5]. Proteomics provided consistent information in revealing proteome alterations associated with GC, dissected some of the mechanisms underlying gastric cancerogenesis, and enabled the identification of several diagnostic, prognostic, and predictive biomarkers [6,7,8,9]. Venous thromboembolism (VTE) has been implicated in GC progression and metastasis [11,12,13,14]. Relevant VTE in GC patients shows an incidence of >5% at 1 year post diagnosis and 12–17% at 2 years, increasing to 24.4% in metastatic advanced GC [15,16,17]
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